Intracellular transport and esterification of exchangeable cholesterol in cultured human lung fibroblasts.
Identifieur interne : 001131 ( Ncbi/Merge ); précédent : 001130; suivant : 001132Intracellular transport and esterification of exchangeable cholesterol in cultured human lung fibroblasts.
Auteurs : J P Slotte ; B. Lundberg ; S. BjörkerudSource :
- Biochimica et biophysica acta [ 0006-3002 ] ; 1984.
Descripteurs français
- KwdFr :
- MESH :
- métabolisme : Cholestérol, Cholestérol ester, Phospholipides, Poumon.
- pharmacologie : Colchicine, Cyanures, Cytochalasine B, Fluorures.
- Cellules cultivées, Humains, Pinocytose.
English descriptors
- KwdEn :
- MESH :
- chemical , metabolism : Cholesterol, Cholesterol Esters, Phospholipids.
- chemical , pharmacology : Colchicine, Cyanides, Cytochalasin B, Fluorides.
- drug effects : Pinocytosis.
- metabolism : Lung.
- Cells, Cultured, Humans.
Abstract
We have studied the intracellular fate of exchangeable cholesterol in a model system with lipid vesicles (cholesterol/phospholipid mole ratio 1:1) and cultured human lung fibroblasts. Exchangeable [3H]cholesterol in lipid vesicles was readily incorporated into cellular plasma membranes and transported to intracellular esterification sites. The formation of [3H]cholesteryl esters was not affected by cytoskeleton-disrupting drugs. A reduction of cellular pinocytosis by 75% did not reduce the formation of tracer-labelled esters, suggesting that membrane flow due to the energy-dependent pinocytosis is no major contributor to the intracellular transport of molecular cholesterol between plasma membranes and esterification sites. The formation of [3H]cholesteryl esters was not significantly affected by energy poisons (NaF and KCN) but was inhibited (to 50%) by chloroquine at 50 microM. This may indicate that membrane-derived cholesterol passes through the lysosomal compartment on its way to intracellular esterification sites.
DOI: 10.1016/0005-2760(84)90258-3
PubMed: 6712979
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Exchangeable [3H]cholesterol in lipid vesicles was readily incorporated into cellular plasma membranes and transported to intracellular esterification sites. The formation of [3H]cholesteryl esters was not affected by cytoskeleton-disrupting drugs. A reduction of cellular pinocytosis by 75% did not reduce the formation of tracer-labelled esters, suggesting that membrane flow due to the energy-dependent pinocytosis is no major contributor to the intracellular transport of molecular cholesterol between plasma membranes and esterification sites. The formation of [3H]cholesteryl esters was not significantly affected by energy poisons (NaF and KCN) but was inhibited (to 50%) by chloroquine at 50 microM. This may indicate that membrane-derived cholesterol passes through the lysosomal compartment on its way to intracellular esterification sites.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">6712979</PMID><DateCompleted><Year>1984</Year><Month>06</Month><Day>18</Day></DateCompleted><DateRevised><Year>2019</Year><Month>06</Month><Day>09</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0006-3002</ISSN><JournalIssue CitedMedium="Print"><Volume>793</Volume><Issue>3</Issue><PubDate><Year>1984</Year><Month>May</Month><Day>11</Day></PubDate></JournalIssue><Title>Biochimica et biophysica acta</Title><ISOAbbreviation>Biochim. Biophys. Acta</ISOAbbreviation></Journal><ArticleTitle>Intracellular transport and esterification of exchangeable cholesterol in cultured human lung fibroblasts.</ArticleTitle><Pagination><MedlinePgn>423-8</MedlinePgn></Pagination><Abstract><AbstractText>We have studied the intracellular fate of exchangeable cholesterol in a model system with lipid vesicles (cholesterol/phospholipid mole ratio 1:1) and cultured human lung fibroblasts. Exchangeable [3H]cholesterol in lipid vesicles was readily incorporated into cellular plasma membranes and transported to intracellular esterification sites. The formation of [3H]cholesteryl esters was not affected by cytoskeleton-disrupting drugs. A reduction of cellular pinocytosis by 75% did not reduce the formation of tracer-labelled esters, suggesting that membrane flow due to the energy-dependent pinocytosis is no major contributor to the intracellular transport of molecular cholesterol between plasma membranes and esterification sites. The formation of [3H]cholesteryl esters was not significantly affected by energy poisons (NaF and KCN) but was inhibited (to 50%) by chloroquine at 50 microM. This may indicate that membrane-derived cholesterol passes through the lysosomal compartment on its way to intracellular esterification sites.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Slotte</LastName><ForeName>J P</ForeName><Initials>JP</Initials></Author><Author ValidYN="Y"><LastName>Lundberg</LastName><ForeName>B</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Björkerud</LastName><ForeName>S</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Biochim Biophys Acta</MedlineTA><NlmUniqueID>0217513</NlmUniqueID><ISSNLinking>0006-3002</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D002788">Cholesterol Esters</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D003486">Cyanides</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D010743">Phospholipids</NameOfSubstance></Chemical><Chemical><RegistryNumber>3CHI920QS7</RegistryNumber><NameOfSubstance UI="D003571">Cytochalasin B</NameOfSubstance></Chemical><Chemical><RegistryNumber>97C5T2UQ7J</RegistryNumber><NameOfSubstance UI="D002784">Cholesterol</NameOfSubstance></Chemical><Chemical><RegistryNumber>Q80VPU408O</RegistryNumber><NameOfSubstance UI="D005459">Fluorides</NameOfSubstance></Chemical><Chemical><RegistryNumber>SML2Y3J35T</RegistryNumber><NameOfSubstance UI="D003078">Colchicine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, Cultured</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002784" MajorTopicYN="N">Cholesterol</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D002788" MajorTopicYN="N">Cholesterol Esters</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003078" MajorTopicYN="N">Colchicine</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003486" MajorTopicYN="N">Cyanides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003571" MajorTopicYN="N">Cytochalasin B</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005459" MajorTopicYN="N">Fluorides</DescriptorName><QualifierName UI="Q000494" MajorTopicYN="N">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010743" MajorTopicYN="N">Phospholipids</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D010873" MajorTopicYN="N">Pinocytosis</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1984</Year><Month>5</Month><Day>11</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1984</Year><Month>5</Month><Day>11</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1984</Year><Month>5</Month><Day>11</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">6712979</ArticleId><ArticleId IdType="pii">0005-2760(84)90258-3</ArticleId><ArticleId IdType="doi">10.1016/0005-2760(84)90258-3</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list></list><tree><noCountry><name sortKey="Bjorkerud, S" sort="Bjorkerud, S" uniqKey="Bjorkerud S" first="S" last="Björkerud">S. Björkerud</name><name sortKey="Lundberg, B" sort="Lundberg, B" uniqKey="Lundberg B" first="B" last="Lundberg">B. Lundberg</name><name sortKey="Slotte, J P" sort="Slotte, J P" uniqKey="Slotte J" first="J P" last="Slotte">J P Slotte</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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